Growth in Response to Pressure Overload Survival but Not in Cardiac Hypertrophic Plays a Critical Role in Cardiomyocyte Mitogen-Activated Protein Kinase

نویسندگان

  • Kenneth R. Chien
  • Junji Takeda
  • Masatsugu Hori
  • Satoshi Tatsuhiko Sudo
  • Kenichi Hongo
  • Yoichiro Kusakari
  • Atsuko Nakai
  • Yasushi Matsumura
  • Jun-ichi Miyazaki
  • Yoshihiro Uno
  • Kazunori Kashiwase
  • Masayuki Taniike
  • Toshihiro Takeda
  • Soh Osuka
  • Takashi Morita
  • Gen Kondoh
  • Shungo Hikoso
  • Yoshiharu Higuchi
  • Tetsuya Watanabe
  • Kazuhiko Nishida
  • Osamu Yamaguchi
  • Shinichi Hirotani
  • Tatsuhiko Sudo
  • Satoshi Kurihara
  • Kinya Otsu
چکیده

10.1128/MCB.24.24.10611-10620.2004. 2004, 24(24):10611. DOI: Mol. Cell. Biol. and Kinya Otsu Kurihara, Kenneth R. Chien, Junji Takeda, Masatsugu Hori Satoshi Tatsuhiko Sudo, Kenichi Hongo, Yoichiro Kusakari, Atsuko Nakai, Yasushi Matsumura, Jun-ichi Miyazaki, Yoshihiro Uno, Kazunori Kashiwase, Masayuki Taniike, Toshihiro Takeda, Soh Osuka, Takashi Morita, Gen Kondoh, Shungo Hikoso, Yoshiharu Higuchi, Tetsuya Watanabe, Kazuhiko Nishida, Osamu Yamaguchi, Shinichi Hirotani, Growth in Response to Pressure Overload Survival but Not in Cardiac Hypertrophic Plays a Critical Role in Cardiomyocyte Mitogen-Activated Protein Kinase α p38

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Targeted deletion of the extracellular signal-regulated protein kinase 5 attenuates hypertrophic response and promotes pressure overload-induced apoptosis in the heart.

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Regulator of G-protein signaling 10 (RGS10) is an important member of the RGS family and produces biological effects in multiple organs. We used a genetic approach to study the role of RGS10 in the regulation of pathological cardiac hypertrophy and found that RGS10 can negatively influence pressure overload-induced cardiac remodeling. RGS10 expression was markedly decreased in failing human hea...

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تاریخ انتشار 2004